Presenilin-1突变对RA诱导的PC12细胞生长和凋亡的影响

目的观察PS-1突变型L286V对RA诱导的PC12细胞生长和凋亡的影响。方法运用脂质体介导的基因转染技术建立稳定表达PS-1WT和突变型L286V基因的细胞克隆,采用MTT法、流式细胞仪检测细胞生长曲线、生长周期及细胞凋亡情况。结果(1)PS-1突变型L286V能使RA诱导的PC12细胞增殖指数降低,G1期细胞增多、S期细胞减少;(2)在正常培养条件和无血清培养下,PS-1突变型L286V对RA诱导的PC12细胞均具有促进细胞凋亡的作用,以无血清培养时表现得更为明显。结论PS-1突变型L286V对RA诱导的PC12细胞生长具有抑制作用和促进细胞凋亡的作用。

Effects of presenilin-1 mutation on the proliferation and apoptosis of RA-induced PC12 cells

Objective To investigate the effects of presenilin-1 (PS-1) mutation (L286V) on the proliferation and apoptosis of RA-induced PC12 cells. Methods The cells expressing stably wide-type PS1 (PS1-WT) and mutant L286V were cloned and made with liposome-mediated gene transfection. The MTT assay, flow cytometry and TUNEL method were applied in the research for detecting the growth curves and periods, and cell apoptosis. Results PS-1 mutant L286V could inhibit the proliferation of the RA-induced PC12 cells, the number increasing in G1 phase and decreasing in S phase. Whether there was FBS in the culture fluid or not, PS-1 mutant L286V can accelerate the apoptosis of RA-induced PC12 cells. This action was more evident in the culture without FBS. Conclusion PS-1 mutant L286V plays a role in inhibiting the growth and accelerating the apoptosis of RA-induced PC12 cells.